Cited by 553Neuroscience and Neuropharmacology ResearchNeural dynamics and brain functionMemory and Neural Mechanisms

Differential regulation of neocortical synapses by neuromodulators and activity

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Gil, Ziv, Connors, Barry W, Amitai, Yael·1997·Neuron

Abstract

Synapses are continually regulated by chemical modulators and by their own activity. We tested the specificity of regulation in two excitatory pathways of the neocortex: thalamocortical (TC) synapses, which mediate specific inputs, and intracortical (IC) synapses, which mediate the recombination of cortical information. Frequency-sensitive depression was much stronger in TC synapses than in IC synapses. The two synapse types were differentially sensitive to presynaptic neuromodulators: only IC synapses were suppressed by activation of GABA(B) receptors, only TC synapses were enhanced by nicotinic acetylcholine receptors, and muscarinic acetylcholine receptors suppressed both synapse types. Modulators also differentially altered the frequency sensitivity of the synapses. Our results suggest a mechanism by which the relative strength and dynamics of input and associational pathways of neocortex are regulated during changes in behavioral state.

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Crossref · 10.1016/s0896-6273(00)80380-3

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  • Activation of α4β2 nicotinic acetylcholine receptors on thalamocortical terminals enhances glutamate release in both sensory and association cortex.

    “Activation of α4β2 nAChRs on thalamocortical terminals enhances glutamate release in both sensory and association cortex (Gil et al., 1997; Lambe et al., 2003; Oldford and Castro-Alamancos, 2003), whereas activation of mAChRs on terminals of parvalbumin-expressing interneurons decreases the probability of GABA release onto the perisynaptic compartment of pyramidal neurons, and therefore reduces”
  • Muscarinic acetylcholine receptors located on pyramidal cell axon terminals suppress cortico-cortical transmission.

    “In contrast, mAChRs located on pyramidal cell axon terminals suppress cortico-cortical transmission (Gil et al., 1997; Hsieh et al., 2000; Kimura and Baughman, 1997; Oldford and Castro-Alamancos, 2003).”
  • Stimulation of nAChRs enhances glutamatergic transmission at thalamocortical synapses, thereby enhancing thalamic activation of subsets of cortical neurons.

    “Previous studies have shown that stimulation of nAChRs enhances the glutamatergic transmission at thalamocortical synapses (Gil et al., 1997; Gioanni et al., 1999; Hsieh et al., 2000), thereby enhancing the thalamic activation of subsets of cortical neurons.”

    From Modes and models of forebrain cholinergic neuromodulation of cognition (2011) · cites this paper as Gil et al., 1997

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Authors
Gil, Z., Connors, B. W., & Amitai, Y.
Affiliations
  • Ben-Gurion University of the Negev (IL)
  • Brown University (US)
Corresponding author
Connors, Barry W
Venue
Neuron
Publisher
Elsevier BV
Published
1997-09
Volume
19
Issue
3
Pages
679-686
ISSN
0896-6273 (ISSN-L)
OpenAlex
W2110258654
Cited by
553
References
64
Citations by year
2026: 7 · 2025: 14 · 2024: 7 · 2023: 14 · 2022: 13 · 2021: 21 · 2020: 13 · 2019: 18 · 2018: 20 · 2017: 21 · 2016: 15 · 2015: 24 · 2014: 18 · 2013: 26 · 2012: 27
FWCI
4.86
Type
journal article
Language
en
Open access
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
synaptic plasticity, neocortex, thalamocortical synapses, GABAB receptors, nicotinic acetylcholine receptors, muscarinic receptors, synaptic depression, behavioral state, excitatory synapses
MeSH terms
Animals, Baclofen, Cholinergic Fibers, Mecamylamine, Mice, Inbred Strains, Synaptic Transmission, Neurons, Afferent, Nicotine, Organophosphorus Compounds, Synapses, Thalamus, Rats, Wistar, Pyramidal Cells, Neurotransmitter Agents, Muscarinic Agonists, Nicotinic Agonists, Nicotinic Antagonists, GABA Agonists, GABA Antagonists, Neocortex, Mice, Rats, GABA-B Receptor Agonists

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